Circulation, Vol 84, 2485-2494, Copyright © 1991 by American Heart Association
MW Keller, L Geddes, W Spotnitz, S Kaul and BR Duling
BACKGROUND. Cardioplegic solutions have been used to enhance myocardial
preservation during cardiac surgery. The benefits derived from preventing
myocardial ischemia with cardioplegic solutions may, however, be countered
by tissue damage that occurs when the myocardium is reperfused with
oxygenated blood. Furthermore, cardioplegia-induced endothelial dysfunction
may contribute to depressed myocardial function postoperatively. The
endothelium of coronary arteries and vein grafts is damaged by crystalloid
cardioplegic solutions. There is less known about the effects of
cardioplegic solutions on the microvasculature. METHODS AND RESULTS. The
hypothesis that microvascular damage occurs following perfusion with
hyperkalemic, crystalloid, cardioplegic solutions and blood reperfusion,
leading to decreased blood flow and increased neutrophil accumulation, was
tested in a model system. Intravital microscopic observations were
performed during a 20-minute perfusion of the hamster cremaster muscle with
cardioplegic solutions (10 degrees C) via the femoral artery with the iliac
occluded and during a subsequent 2-hour blood reperfusion period (iliac
open). Arteriolar vasoconstriction (27% decrease in diameter, p less than
0.05) and a 25% decrease in the density of perfused capillaries (p less
than 0.05) occurred during reperfusion in hamsters receiving crystalloid
cardioplegic solution (16 meq K+) compared to control hamsters (no
cardioplegic solution given). Neutrophils accumulated on venular
endothelium in treated animals (250% increase, p less than 0.05) and
extravascularly (myeloperoxidase levels 2.0 +/- 0.4 U/g versus 1.3 +/- 0.3
U/g in control, p less than 0.05). The addition of adenosine (10(-4) M) and
albumin (2 g%) to the cardioplegic perfusate, accompanied by the
administration of adenosine (10(-4) M) during reperfusion, produced
arteriolar vasodilation (34% diameter increase, p less than 0.05) and
inhibited extravascular neutrophil accumulation (myeloperoxidase level of
1.5 +/- 0.2 U/g, p greater than 0.05 versus control). Capillary perfusion,
however, was still significantly diminished (28% decrease, p less than
0.05.) CONCLUSIONS. We conclude that injury manifest by decreased
microvascular blood flow and increased neutrophil accumulation in tissues
occurs after perfusion with hypothermic, hyperkalemic, crystalloid
cardioplegic solutions and blood reperfusion. Adenosine seems to partially
attenuate this injury by dilating arterioles and decreasing extravascular
neutrophil accumulation.
ARTICLES
Microcirculatory dysfunction following perfusion with hyperkalemic, hypothermic, cardioplegic solutions and blood reperfusion. Effects of adenosine
Department of Medicine, University of Virginia Health Sciences Center, University of Virginia, Charlottesville 22908.
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